ABSTRACT
There is now considerable experimental and clinical evidence supporting the supposition that overactivity of the bladder is associated with detectable alterations in the electrical properties of the detrusor smooth muscle cells. The preliminary data described in this report indicates that intercellular communication through gap junctions might play an important role in this process. Moreover, alterations in Cx43 mRNA expression may represent a tissue response to a physiologic insult (i.e., increased after load) in an attempt to further increase the syncytial nature and force of detrusor contractility to compensate for an increased pressure load. Finally, this report elucidates the rationale for suspecting that intercellular communication through gap junctions may play a role in normal bladder physiology and the pathophysiology of urinary incontinence caused by partial outlet obstruction.
